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Biomedical subjects

C B Brown

Publications and source records attributed to C B Brown.

At least 109 records · Page 6Linked to original sources
PubMed1987

Glomerulonephritis and IgA deficiency.

A mild self-limiting mesangial proliferative glomerulonephritis is described in 3 patients with selective IgA deficiency (less than 0.05 g/l). In all cases there was irregular thickening of peripheral glomerular capillary loops and paramesangial deposits. Arteriolar hyalinosis was present in two of the three cases. By direct immunofluorescence, and immunoperoxidase techniques in one case, IgM was present in the glomeruli and C3 was present in blood vessel walls. Secretory component was not detected in the glomeruli of any of the patients. The polyethylene glycol (PEG) precipitation immune complex assay was positive for IgM and IgG immune complexes in one patient and weakly positive for IgM immune complexes alone in another. The serum of one patient contained milk precipitins. All three patients had suffered from recurrent upper respiratory tract infections. It is suggested that the glomerular IgM immune complex deposition is related to the IgA deficiency and that, although the immune complexes may be a consequence of antibodies to dietary bovine proteins, this could be due to recurrent upper respiratory tract infections. This type of glomerulonephritis appears to resemble IgM associated glomerulonephritis in some aspects. Careful appraisal is required to establish if this association constitute a specific entity.

Adult↗
PubMed1986

Evidence against a platelet cyclooxygenase defect in uraemic subjects on chronic haemodialysis.

Defective platelet thromboxane synthesis has been described in uraemia and attributed to a 'functional cyclooxygenase defect'. We have studied platelet aggregation and generation of immunoreactive thromboxane B2 (TXB2) in 11 subjects on a chronic haemodialysis programme. The platelet function abnormality of uraemia was confirmed, maximal aggregation in response to collagen (2 and 4 micrograms/ml) and sodium arachidonate (1.5 and 3.0 mM) being significantly depressed. However, increased platelet aggregation in response to sodium arachidonate 0.75 mM was noted. Due to the reduced haematocrit, the platelet concentration in platelet-rich plasma (PRP) of uraemic subjects was significantly lower than that of controls; when TXB2 generation in PRP adjusted to 200 X 10(9) platelets/l was assessed, no evidence for a defect of cyclooxygenase was found, although reduced synthesis of TXB2 in response to thrombin was noted. Furthermore, increased thromboxane generation by uraemic PRP in response to sodium arachidonate 0.75 mM was detected. We conclude that the mild platelet abnormality in uraemic subjects treated by haemodialysis is not explained by a 'functional cyclooxygenase defect', although an abnormality of thrombin-induced thromboxane synthesis may be present. Furthermore, the tendency to increased aggregation and thromboxane synthesis in response to a low concentration of arachidonic acid may contribute to the thrombotic tendency which is also described in such subjects.

Adult↗
PubMed1986

Protein losing enteropathy as a sole manifestation of non-Hodgkin's lymphoma.

We describe a patient who presented with oedema and hypoproteinaemia which was proved to be due to protein-losing enteropathy. Extensive gastrointestinal investigations failed to discover any definitive cause. He subsequently developed tuberculous inguinal lymphadenopathy but although treated for tuberculosis the protein-losing state persisted. Later on he developed renal failure due to obstructive nephropathy. Laparotomy was carried out and it disclosed the diagnosis of non-Hodgkin's lymphoma, treatment of which cured the protein-losing state.

Adult↗
PubMed1986

Renal micropolyarteritis: a treatable condition.

A 10-year retrospective study of 36 patients is presented; the patients comprised 27 with renal micropolyarteritis nodosa (microPAN) and nine with Wegener's granulomatosis. At presentation, 29 patients had significant renal impairment (creatinine greater than 150 mumol/l), with 18 requiring dialysis at some time during their illness. Eighteen patients showed rapid recovery of renal function, a further two with apparently chronic renal failure recovered renal function after 4 months dialysis and continued immunosuppression. Seven patients required chronic dialysis. No benefit was shown for any particular immunosuppressive regime, with three patients recovering renal function (two initially on dialysis) without any immunosuppression. Prognosis was better than in previous published series, especially considering the elderly population (mean 52.9 years), with an 80% 1-year and a 64% 5-year survival.

Anti-Inflammatory Agents↗
PubMed1986

An assessment of intrarenal hydrostatic pressure measurements in the diagnosis of acute renal allograft rejection.

Postoperative intrarenal pressure measurements may be an aid to the diagnosis of acute renal transplant rejection, especially in patients treated with cyclosporine. Serial measurements of intrarenal pressure were made in 38 recipients using a fine-needle technique. Thirty-two intraoperative and 207 postoperative measurements were made, and 39 clinical rejection episodes (23 confirmed by biopsy) monitored. Intraoperative pressures in grafts with immediate function (37.4 +/- 4.0 mmHg, mean +/- SEM) were not significantly different from those with delayed function (30.9 +/- 4.8 mmHg), whereas postoperative pressures were greater (P less than 0.01) in kidneys with acute tubular necrosis (29.4 +/- 1.9 mmHg) than in functioning grafts (20.4 +/- 0.9 mmHg). Pressures recorded during clinical rejection episodes (44.3 +/- 2.3 mmHg) exceeded (P less than 0.001) those during quiescent periods (23.6 +/- 1.0 mmHg). During rejection episodes, higher pressures (P less than 0.01) were recorded from tender or palpably enlarged grafts (52.5 +/- 3.0 mmHg) than in the absence of these signs (36.3 +/- 3.1 mmHg), and patients whose transplants biopsies showed cellular rejection tended to have greater pressures (50.1 +/- 4.1 mmHg) than those with concomitant vasculopathy (36.4 +/- 3.9 mmHg), but the latter did not reach statistical significance. In 7 cases of cyclosporine toxicity the intrarenal pressure was 17.8 +/- 4.2 mmHg. Using a diagnostic cut off point of 40 mmHg, the investigation failed to recognize 26% of acute rejection episodes--and, in the presence of acute tubular necrosis, it wrongly categorized 21% of nonrejectors. While its predictive capacity was limited, the test may occasionally be helpful in the differentiation of cyclosporine toxicity and rejection in functioning kidneys.

Acute Kidney Injury↗
PubMed1985

IgE against ethylene oxide-altered human serum albumin in patients with anaphylactic reactions to dialysis.

We have measured total antibody and IgE directed against ethylene oxide-altered human serum albumin (ETO-HSA) in the sera of 24 patients who have experienced anaphylaxis during hemodialysis and of 41 patients who have not had such episodes during hemodialysis. ETO is used to sterilize dialyzers and other medical equipment. The geometric mean level of IgE to ETO-HSA in patients with reactions (0.9 ng ETO-HSA bound to IgE per milliliter of serum) is significantly higher than in nonreacting patients (0.1 ng/ml, p less than 0.0001). Sixteen of 24 patients with reactions had detectable levels of IgE to ETO-HSA, whereas only three of 41 nonreacting patients had detectable levels (p less than 0.0001 chi-square). The geometric mean level of total antibody to ETO-HSA is also significantly higher in patients with reactions (270 ng ETO-HSA bound per milliliter) than in nonreacting patients (31 ng/ml, p less than 0.0001). Fourteen of 24 patients with reactions but only four of 39 nonreacting patients had total antibody binding of ETO-HSA (p less than 0.0001 chi-square). These data extend our previous observations on a small group of 13 patients receiving hemodialysis (seven patients with reactions, and six nonreacting patients) and clearly demonstrate an association between the presence of IgE or total antibody to ETO-HSA and immediate anaphylactic reactions in this group of 65 patients receiving hemodialysis.

Anaphylaxis↗
PubMed1985

Hemolytic-uremic syndrome: demonstration of abnormalities of platelet reactivity and insensitivity to prostaglandin I2.

Platelet aggregation and thromboxane synthesis and platelet sensitivity to the antiaggregatory action of prostaglandin I2 were studied serially in a subject suffering from adult hemolytic-uremic syndrome. Platelet aggregation in vitro was defective during the acute phase of the disease and recovered during the convalescent phase. Defective aggregation was not associated with a failure of thromboxane synthesis although it was related to an intrinsic platelet defect rather than an inhibitor in the plasma. The platelets were insensitive to prostaglandin I2, even in the recovery phase of the disease. Furthermore, plasma from the patient rendered normal platelets insensitive to prostaglandin I2 and more sensitive to aggregating agents. It is concluded that the platelet abnormality in hemolytic-uremic syndrome is complex and it combines both an intrinsic platelet abnormality and a plasma component.

Acute Disease↗
PubMed1984

Impact of continuous ambulatory peritoneal dialysis on treatment of renal failure in patients aged over 60.

Thirty eight patients aged over 60 with end stage renal disease were treated by continuous ambulatory peritoneal dialysis for up to three years. Most of these patients, because of their age or coexisting diseases, had been considered to be unsuitable for haemodialysis by the criteria used before the advent of continuous ambulatory peritoneal dialysis in 1980. Actuarial patient survival at one and two years was 72% and 61% respectively, and only two patients were permanently transferred to haemodialysis. Twenty one of the 23 survivors were fully rehabilitated, the remaining two being partially disabled but living at home. Continuous ambulatory peritoneal dialysis permits more liberal selection of patients with end stage renal disease for renal replacement treatment with excellent survival and rehabilitation and without overburdening scarce hospital haemodialysis facilities.

Aged↗